Molekulargenetisches Labor
Zentrum für Nephrologie und Stoffwechsel
Moldiag Erkrankungen Gene Support Kontakt

Vererbte Magersucht

Bei der vererbte Magersucht liegt eine erblich bedingter besonders schlanker Körperbau vor. Es handelt sich vor allem um eine Ausschlussdiagnose, wobei differentialdiagnostisch Essstörungen und generalisierte Lipodystrophien abzugrenzen sind. Die Störung wird durch Mutationen im AGRP-Gen verursacht.

Gliederung

Störung der Körperfettverteilung
Fettleibigkeit
Lipodystrophie
Vererbte Magersucht
AGRP

Referenzen:

1.

Kitamura T et al. (2006) Forkhead protein FoxO1 mediates Agrp-dependent effects of leptin on food intake.

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2.

Shutter JR et al. (1997) Hypothalamic expression of ART, a novel gene related to agouti, is up-regulated in obese and diabetic mutant mice.

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3.

Ollmann MM et al. (1997) Antagonism of central melanocortin receptors in vitro and in vivo by agouti-related protein.

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4.

Graham M et al. (1997) Overexpression of Agrt leads to obesity in transgenic mice.

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5.

Katsuki A et al. (2001) Plasma levels of agouti-related protein are increased in obese men.

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6.

Brown AM et al. (2001) The gene structure and minimal promoter of the human agouti related protein.

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7.

Argyropoulos G et al. (2002) A polymorphism in the human agouti-related protein is associated with late-onset obesity.

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8.

Marks DL et al. (2004) Ala67Thr polymorphism in the Agouti-related peptide gene is associated with inherited leanness in humans.

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9.

Luquet S et al. (2005) NPY/AgRP neurons are essential for feeding in adult mice but can be ablated in neonates.

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10.

Andrews ZB et al. (2008) UCP2 mediates ghrelin's action on NPY/AgRP neurons by lowering free radicals.

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11.

Atasoy D et al. (2012) Deconstruction of a neural circuit for hunger.

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12.

Krashes MJ et al. (2014) An excitatory paraventricular nucleus to AgRP neuron circuit that drives hunger.

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13.

OMIM.ORG article

Omim 602311 external link
Update: 14. August 2020
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